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Intestinal Metallothionein Gene Expression and Zinc Absorption in Rats Are Zinc-Responsive but Refractory to Dexamethasone and Interleukin 1¹

Food Science and Human Nutrition Department ^* Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Florida, Gainesville, FL 32611

The effects of dexamethasone and interleukin 1 on intestinal metallothionein gene expression and zinc absorption were studied. Rats given parenteral zinc served as positive controls. A single intraperitoneal or intravenous dose of dexamethasone, interleukin 1 or zinc markedly increased liver metallothionein synthesis 3–9 h after injection. Intestinal metallothionein mRNA and metallothionein protein were not affected by dexamethasone or interleukin 1, but were markedly increased by parenteral zinc. Absorption of ⁶⁵Zn from isolated duodenal segments was inversely related to intestinal metallothionein concentration in rats given zinc, but was not affected by dexamethasone or interleukin 1. Plasma zinc concentrations decreased in rats given dexamethasone or interleukin 1 and increased in those given zinc, but they were not related to ⁶⁵Zn absorption. Similarly, multiple intraperitoneal administration of either dexamethasone or interleukin 1, or oral administration of dexamethasone, for 7 d markedly increased liver metallothionein synthesis but did not affect intestinal metallothionein concentration or ⁶⁵Zn absorption. These results suggest that intestinal metallothionein gene expression and ⁶⁵Zn absorption are refractory to glucocorticoid hormone and interleukin 1.

KEY WORDS: • zinc • metallothionein • glucocorticoid hormone • interleukin 1 • rats

¹ Supported by National Institutes of Health Grant DK 31127 and Boston Family Endowment Funds.

² Recipient of National Research Service Award DK 08276.

³ Supported in part by a Clinical Nutrition Fellowship from the Center for Nutritional Sciences of the University of Florida.

⁴ To whom correspondence should be addressed.

Manuscript received 24 September 1990. Revision accepted 18 February 1991.

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